Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

MULTI VALVULAR HEART DISEASE clinical presentation

5,490 views

Published on

APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS

Published in: Health & Medicine
  • If you want to download or read this book, copy link or url below in the New tab ......................................................................................................................... DOWNLOAD FULL PDF EBOOK here { https://urlzs.com/UABbn } .........................................................................................................................
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • If you want to download or read this book, Copy link or url below in the New tab ......................................................................................................................... DOWNLOAD FULL PDF EBOOK here { http://bit.ly/2m77EgH } ......................................................................................................................... Download EPUB Ebook here { http://bit.ly/2m77EgH } ......................................................................................................................... Download Doc Ebook here { http://bit.ly/2m77EgH } ......................................................................................................................... .........................................................................................................................
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • DOWNLOAD FULL. BOOKS INTO AVAILABLE FORMAT ......................................................................................................................... ......................................................................................................................... 1.DOWNLOAD FULL. PDF EBOOK here { https://tinyurl.com/y8nn3gmc } ......................................................................................................................... 1.DOWNLOAD FULL. EPUB Ebook here { https://tinyurl.com/y8nn3gmc } ......................................................................................................................... 1.DOWNLOAD FULL. doc Ebook here { https://tinyurl.com/y8nn3gmc } ......................................................................................................................... 1.DOWNLOAD FULL. PDF EBOOK here { https://tinyurl.com/y8nn3gmc } ......................................................................................................................... 1.DOWNLOAD FULL. EPUB Ebook here { https://tinyurl.com/y8nn3gmc } ......................................................................................................................... 1.DOWNLOAD FULL. doc Ebook here { https://tinyurl.com/y8nn3gmc } ......................................................................................................................... ......................................................................................................................... ......................................................................................................................... .............. Browse by Genre Available eBooks ......................................................................................................................... Art, Biography, Business, Chick Lit, Children's, Christian, Classics, Comics, Contemporary, Cookbooks, Crime, Ebooks, Fantasy, Fiction, Graphic Novels, Historical Fiction, History, Horror, Humor And Comedy, Manga, Memoir, Music, Mystery, Non Fiction, Paranormal, Philosophy, Poetry, Psychology, Religion, Romance, Science, Science Fiction, Self Help, Suspense, Spirituality, Sports, Thriller, Travel, Young Adult,
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

MULTI VALVULAR HEART DISEASE clinical presentation

  1. 1. MULTI VALVULAR HEART DISEASE PROF.M.K.SUDHAKAR SRMC
  2. 2. OBJECTIVES  A CLINICAL SHORT CASE DISCUSSION  APPROACH TO THE VARIOUS MULTIVALVULAR HEART DISEASES IN CLINICAL GROUNDS.
  3. 3. CASE PRESENTATION.
  4. 4. GENERAL EXAMINATION  46 yr / male  Conscious , Oriented to time, place and person  Weight – 60 kg  Height – 162.5 cm  Arm span – 145 cm  BMI – 22.8 kg/m2
  5. 5.  Vitals  Temperature - 98.2 F  Pulse  80/min, Regular,  large volume,  Collapsing in nature(water hammer pulse)  Bis feriens in character,  Carotid thrill +.  Normal vessel wall  No radio-radial or radio-femoral delay  All peripheral pulses are well felt  No apex- pulse deficit noted.
  6. 6.  110/50 mm of Hg over right brachial artery in supine position  110/50mm of Hg over Lt. brachial artery  Systolic BP measured in lower limb is 160 mm of Hg  Hill’s sign - positive ( systolic BP difference between upper & lower limbs is 50 ) Blood Pressure
  7. 7.  JVP – elevated 5 cms above the sternal angle, but the waveforms masked by carotid pulsations in neck.  Respiration - Rate- 17/min, Regular, Abdomino-thoracic type  No other peripheral signs of AR.  No P I C C L E.  No external markers of Rheumatic fever / Infective Endocarditis  Fundus Examination – Normal
  8. 8. CARDIOVASCULAR SYSTEM
  9. 9. INSPECTION  Chest symmetrical, no spinal or chest deformity noted  Trachea appears to be in midline  Carotid pulsations are visible in the neck.  Apical impulse is visible in left 5th intercostal space in Midclavicular line confined to single intercostal space.  Visible pulsations noted in left parasternal area.  Parasternal heave is visible.  No sinus , dilated veins over chest wall.  A healed surgical scar of 15 cms in the left thoracic wall extending from mid clavicular line(6 ICS) to the post axillary line.
  10. 10. PALPATION  Trachea centrally placed.  Apex beat localized in the Left 5th Intercostal space Midclavicular line confined to single Intercostal space, tapping in nature, systolic thrill palpable.  Parasternal heave felt and not obliterable (grade 3)  Systolic thrill noted in aortic area and all over precordium.  Palpable P2 noted in pulmonary area.  Supra sternal and epigastric pulsations are felt.
  11. 11. Aortic Area  S1 heard  A2 soft.  A harsh ejection systolic murmur occupying almost of entire systole ; crescendo-decrescendo in nature with delayed peaking, of grade 4 intensity conducted to both carotids which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration  No ejection click noted.  Dynamic auscultation:  murmur is augmented on squatting  Reduces on standing and isometric hand grip.
  12. 12.  Pulmonary Area:  S1heard  P2 loud and s2 single.  Systolic Crescendo decrescendo murmur same as heard in aortic area best heard in expiration with pt leaning forward.  No ejection click noted.  Dynamic auscultation:  murmur is augmented on expiration; squatting and reduced on isometric hand grip.
  13. 13. 2nd Aortic Area ( Erb’s Area )  S1 heard  A2 soft  A harsh ejection systolic murmur occupying almost of entire systole ; crescendo-decrescendo in nature with delayed peaking, of grade 4 intensity conducted to both carotids which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration
  14. 14.  A grade 3 high pitched , blowing , early diastolic decrescendo murmur which is best audible with diaphragm of stethoscope in sitting and leaning forward position with breath held in expiration .  No ejection click noted.  Dynamic auscultation:  The early diastolic murmur is augmented on isometric hand grip and expiration.
  15. 15.  Tricuspid Area:  S1 , S2 heard  A High pitched Pan systolic murmur grade 4 intensity ;best heard with the diaphragm which increases on inspiration is heard.  No s3,s4 heard.
  16. 16. Mitral Area:  S1 S2 heard.  S1 loud.  Low pitched rough rumbling mid diastolic murmur of grade 3 intensity noted at the apex with the bell of the stethoscope with best heard in left lateral position and pt in expiration.  A high pitched holo systolic murmur is noted of grade 4 intensity radiating from the tricuspid area confirmed by inch auscultation. Which increases on inspiration.  No opening snap heard.  No s3 ,s4 heard.
  17. 17. OTHER SYSTEMS  Respiratory System:  Bilateral normal vesicular breath sounds heard  No added sounds  Abdominal System:  Soft , Non tender , No organomegaly  No ascites  Nervous System:  No focal neurological deficit
  18. 18. CLINICAL DIAGNOSIS  Anatomical: Mitral and Aortic valves with tricuspid valve.  Etiology :Acquired Rheumatic Valvular Heart Disease  Pathological:  Severe mitral re stenosis  Severe aortic stenosis  Moderate aortic regurgitation  Functional tricuspid regurgitation.  Complication : Pulmonary hypertension  Patient is in sinus rhythm  No evidence of Cardiac failure  No evidence of Infective endocarditis  No evidence of Thromboembolic event
  19. 19. 1.What are the common causes of Multivalvular heart diseases ?
  20. 20.  Multivalvular lesions are almost always due to Rheumatic fever  Collagen vascular diseases or myxomatous degeneration are rare causes
  21. 21.  Significant stenosis at multiple valves are usually Rheumatic  Significant regurgitation at multiple valves are usually Non Rheumatic  Significant stenosis and regurgitation together are usually rheumatic.
  22. 22. MVD  Quadrivalvular disease is most likely due to combination of causes – congenital , rheumatic, infective, degenerative disease  A unitary cause for quadrivalvular disease is either rheumatic or myxomatous degeneration
  23. 23. 2.What are the factors which modify the clinical presentation of MVD ?
  24. 24.  The natural history and clinical presentation of combined lesions is determined by the relative severity of each individual lesion and by chronology and chronicity of development  Proximal lesions mask the features of distal lesions
  25. 25. Non valvular Factors  Myocarditis  Volume overload states  Pressure overload states  CAD  Infective endocarditis  Arrhythmias
  26. 26.  WHEN DO U SUSPECT A MVD ?
  27. 27. MVD  Atrial fibrillation  Pulmonic hypertension  Pulmonic congestion  Systemic emboilsm
  28. 28. What is graham steel murmur?  What are the recent views on it?
  29. 29. Features of Combined AS/AR:
  30. 30. AS + AR  Apico carotid delay  S2 paradoxical split  A2 – soft or absent  S3  S4
  31. 31.  Prolonged Aortic ESM  Prolonged Aortic EDM  Austin Flint Murmur
  32. 32. Dominant AS vs Dominant AR
  33. 33. DOMINANT AS Anacrotic pulse Apex heave Systolic decapitation Systolic Ejection Click
  34. 34.  S2 reverse split  S3 – later  S4  Systolic murmur – late, loud, longer
  35. 35. DOMINANT AR  Wide pulse pressure  Pulsus bisferiens  Diffuse apical impulse  Early diastolic murmur  S3 – earlier
  36. 36. What is silent AS, severe AS?
  37. 37. SILENT AS Old age – non fused, calcified cusps Cardiac failure Severe AS AS + MS
  38. 38. SEVERE AS JVP a wave (Bernheim effect) Apico carotid delay S2 single or paradoxical split AEC absent S4 Systolic murmur - late, loud, longer Mitral pansystolic functional murmur
  39. 39. What is silent AR, severe AR?
  40. 40. SEVERE AR  Hills sign > 60 mm hg  S2 soft  S3  EDM – louder & longer  Cole Cecil murmur  Austin Flint murmur
  41. 41.  Cole Cecil murmur – AR EDM heard in the apex or axilla  Austin Flint murmur – MDM heard in severe and acute AR
  42. 42. SILENT AR  Acute AR  CCF  AR + AS  AR + MS
  43. 43. COMBINED MITRAL LESION:
  44. 44. MS + MR  Mitral valve orifice < 1.5 sq.cm MS is predominant  Mitral valve orifice > 1.5 sq.cm MR is predominant
  45. 45. MS + MR  Parasternal heave - prominence  Apical impulse - prominence  Apical MDM  Apical PSM
  46. 46. DOMINANT MS ?
  47. 47. DOMINANT MS  Parasternal lift – early systolic & brisker  Tapping apical impulse  S1 - loud  OS  MDM/LDM
  48. 48. DOMINANT MR?
  49. 49. DOMINANT MR  Parasternal impulse – slower & late systolic  Hyperdynamic apical impulse  Pansystolic murmur  S1 - soft  S3
  50. 50. WHAT IS…..  SILENT MS?  SEVERE MS?
  51. 51. SILENT MS  Severe MS with pulmonary hypertension RV enlarges and LV rotates clockwise - tight or silent MS  TS + MS  AS + MS
  52. 52. SEVERE MS  A2 OS interval - closer  MDM – longer  Severe PHT
  53. 53. What is  Silent MR?  Severe MR?
  54. 54. SILENT MR  Obesity  Emphysema  Chest wall deformity  LV infarction / dilatation  Para prosthetic leakage
  55. 55. SEVERE MR  S1 – soft  S2 – wide and variable  S3  PSM – intensity  MDM – short low pitch flow murmur.
  56. 56. MS + AS  The combination of Mitral stenosis and Aortic stenosis is almost always due to rheumatic  The combinations is usually associated with significant regurgitation at either valve  Mitral stenosis masks Aortic stenosis
  57. 57. MS + AS  Carotid pulse & Apex prominent  Parasternal heave  Loud S1  OS  Ejection systolic murmur Grade < 3/6  Mid diastolic murmur
  58. 58. MS < AS  Angina  Syncope  Carotid thrill  Apical impulse heave  Ejection systolic murmur
  59. 59. MS > AS  Dyspnea  Pulmonic hypertension  Atrial fibrillation  Systemic thromboembolism  MDM
  60. 60. MS + AR  Wide pulse pressure  Apical prominence  Parasternal impulse  Loud S1  OS  S3 S4
  61. 61.  Early diastolic murmur  Mid diastolic murmur
  62. 62. MR + AS  Geriatric – calcific  Rheumatic
  63. 63. MR + AS  AS augments the severity of MR  Systemic hypotension  Pulmonic hypertension
  64. 64. MR + AS  Hyperdynamic AI  S3 / S4  Mitral – PSM  Aortic – ESM
  65. 65. MR < AS  Angina  Syncope  Fatigue
  66. 66.  Carotid thrill  S4  Systolic murmur decreased on squatting or hand gripping
  67. 67. MR = AS  Angina  Dyspnea  Syncope  Fatigue  Pulmonic congestion  Systemic embolism
  68. 68.  Atrial fibrillation  Carotid thrill  Diffuse & sustained apical impulse  S2 soft  S3  S4
  69. 69. WHAT IS GALLIVARDIAN PHENOMENON?
  70. 70. GALLIVARDIAN PHENOMENON  An acoustic phenomenon whereby the aortic ejection systolic murmur radiates to the mitral area with reduced intensity but prolonged duration so as to be heard as a pansystolic murmur  AS often confused with MR
  71. 71.  Inch auscultation along the sash line appreciates the transformation  Sash line is an imaginary line through right carotid, aortic area, second aortic area ,mitral area
  72. 72. MR + AR  Most common cause is rheumatic with or without AS / MS  Pure MR and AR is due to connective tissue disorders with myxomatous degeneration of valve tissue when TR coexists  Infective endocarditis or chordal rupture produce regurgiation in congenital or rheumatic valve diseases
  73. 73.  When MR > AR , it attenuates AR  When AR > MR , it worsens MR  Pulmonary symptoms are earlier and severe with MR + AR combination than in isolation
  74. 74. MR + AR  MR is worsened by AR  Wide pulse pressure  Peripheral signs  Diffuse apical impulse
  75. 75.  P2  S3  S4  Mitral PSM  Aortic EDM
  76. 76. MR < AR  Wide pulse pressure  Longer EDM  Longer PSM  S4
  77. 77. MR = AR  Wide pulse pressure  Parasternal heave  Longer EDM  Longer PSM
  78. 78. MR > AR  Atrial fibrillation  Parasternal heave  Longer PSM
  79. 79. AS / AR / MS /MR  Rheumatic  Murmurs of all four hemodynamic lesions  Pulmonary congestion
  80. 80. TVD
  81. 81. TS  TS is very unusual as an isolated lesion  TS is almost always due to rheumatic valvulitis and is associated with coexisting disease of mitral and aortic valves  TS almost always coexists with MS and only rarely with predominant MR
  82. 82.  MS precedes TS  TS masks MS  TS is to be suspected when RHF persists after adequate mitral valvotomy
  83. 83. TR  Functional TR is more frequent than organic TR and is due to severe Pulmonary hypertension  Severe organic TR is almost always due to rheumatic origin and accompanies TS  Severe organic TR coexists with Mitral or Aortic valve disease
  84. 84. TS > TR  Tricuspid OS  The Tricuspid diastolic murmur increases and whereas Tricuspid systolic murmur decreases with inspiration
  85. 85. TR > TS  Tricuspid S3  The Tricuspid diastolic murmur decreases and whereas Tricuspid systolic murmur increases with inspiration
  86. 86. PVD  Pulmonic valve disease is unusual in rheumatic heart disease , when it occurs it is usually in quadrivalvular disease  Carcinoid tumor should be suspected when pulmonary and tricuspid valve lesions coexist
  87. 87. How will you investigate MVD ? History or Physical examination provides insignificant clues to recognize pulmonary valve disease in multivalvular disease
  88. 88. INVESTIGATIONS:  ECG  CXR  2D ECHO  Cardiac catheterization
  89. 89. How do you manage multivalvular diseases ?
  90. 90.  In Ideal conditions all lesions should be corrected simultaneously  In practice distal lesions are corrected first followed by proximal lesions.
  91. 91. PROCEDURES.  Valvotomy  Valvuloplasty  Valve replacement
  92. 92. THANK YOU……

×